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Abstract:
The hippocampus encodes information relevant to both event memory and spatial navigation. Both alterations in hippocampal function, and memory deficits, are observed in schizophrenia. It is, however, unclear how these hippocampal changes might contribute to the memory problems. To address this question we have modelled aspects of schizophrenia using prenatal maternal immune activation (MIA), which is a known risk factor for the disease, in an animal model. MIA was induced in pregnant rat dams with a single injection of the synthetic cytokine inducer polyinosinic:polycytidylic acid (poly I:C) on gestational day 15. Control dams were given a saline equivalent. Firing activity and local field potentials (LFPs) were recorded from the CA1 region of the hippocampus in adult male offspring of these dams as they moved freely around a rectangular track.
A large proportion of neurons recorded from both groups displayed characteristic spatially-modulated ‘place cell’ firing activity and the burst firing activity that occurs during sharp-wave ripple (SWR) LFP events. SWR bursts have been linked to memory consolidation and anticipatory ‘preplay’ processes. Initial data from our studies indicates that while classic place cell ‘rate code’ firing is relatively unaffected by the MIA intervention, ‘temporal code’ firing is altered. In particular, an analysis of the timing of SWR bursts revealed that they had less coherent structure than was observed in control animals. This effect has the potential to impact on both decision-making and memory consolidation processes. Furthermore, when viewed from a Complementary Learning System approach, a reduction in coherent episodic-semantic memory consolidation might underlie some of the semantic memory deficits observed in schizophrenia.
